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Acute ischemia causes axonal stasis, swelling, attenuation, and secondary demyelination
Author(s) -
Nukada Hitoshi,
Dyck Peter James
Publication year - 1987
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410220306
Subject(s) - axonal degeneration , axon , ischemia , pathology , degeneration (medical) , pathological , medicine , myelin , sciatic nerve , anatomy , central nervous system
Microsphere embolization of rat sciatic nerve capillaries results in a central fascicular ischemic core. Twenty‐four hours after microembolization, the pathological alterations along the length of 55 myelinated fibers were reconstructed by computer imaging of 2,000 serial semi‐thin epoxy sections of a tissue block that extended from just above and into an ischemic core. From proximal to distal, the typical sequence of pathological alternations was: normal → swollen dark axons + thin myelin or demyelination → attenuated axons → axon cytolysis (46 fibers) or normal axons (9 fibers). Because organelle accumulation and axonal swelling were the earliest and most proximal pathological lesions, we infer that regional hypoxia causes axonal stasis as a primary event. Demyelination was found in fibers showing swollen dark and attenuated axons. These findings suggest that axons are selectively vulnerable to acute ischemia and that, depending on severity, the fibers either undergo axonal degeneration or transitory structural alterations without axonal degeneration, the latter consisting of axonal changes and secondary demyelination.